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GI Physiology Flashcards

1
Q

GI System Physiology Two Major Functions:

A

(1) Digestion

(2) Absorption of Nutrients

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2
Q

GI System Physiology Four Activities:

A
  1. Motility
  2. Secretions
  3. Digestion
  4. Absorption
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3
Q

Motility -

Define

A

food propelled from mouth –> rectum

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4
Q

Secretions -

Define

A

pancreatic, salivary and hepatic enzymes and electrolytes help with digestion/absorption

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5
Q

Absorption -

Define

A

–> Blood - absorbed nutrients, electrolytes & water are transferred into the blood stream

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6
Q

Mucosal Layer contains:

A

(Epithelium + Lamina Propria + Muscularis Mucosa)

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7
Q

Mucosal Layer function:

A
  • Epithelium specialized for absorption & secretion

* Contraction of muscularis mucosa = ΔShape & Surface Area of Epithelium

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8
Q

Submucosal Layer contains:

A

(collagen, elastin, glands, blood vessels)

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9
Q

Muscularis Mucosa layer:

A

Circular Muscle

Longitudinal Muscle

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10
Q

Serosal Mucosa layer:

A

(Faces Blood)

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11
Q

Nerve Plexuses

A
  1. Meissner’s Plexus:

2. Myenteric Plexus:

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12
Q

Meissner’s Plexus:

A

Submucosal Plexus (Meissner’s Plexus): deep to submucosal layer

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13
Q

Myenteric Plexus:

A

deep to circular muscle

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14
Q

Enteric Nervous System (ENS):

A

Composed of the Meissner’s Plexus & Myenteric Plexus located on either side of the circular smooth muscle. They comprise the intrinsic innervation of the GI Tract.

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15
Q

Innervation of the GI Tract -

A

Autonomic Nervous System Extrinsic & Enteric System Intrinsic

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16
Q

Extrinsic Innervation include:

A

Parasympathetics & Sympathetics

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17
Q

Parasympathetics Nerves:

A
  1. Vagus Nerve:

2. Pelvic Splanchnic Nerves:

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18
Q

Vagus Nerve:

A

Striated muscle in ↑1/3 of Esophagus, Stomach, Small Intestine & Ascending Colon (= ↑GI Tract)

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19
Q

Pelvic Splanchnic Nerves:

A

Transverse colon, descending + sigmoid colon, & striated muscle of anal canal (= ↓GI Tract)

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20
Q

Parasympathetics have long?

A

Pre-ganglionic fibers that synapse in ganglion INSIDE the submucosal & myenteric plexus

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21
Q

Parasympathetic post-ganglionic fibers relayed to

A

Smooth muscle, endocrine glands & secretory cells.

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22
Q

Parasympathetic Neurotransmitters:

A
  1. Cholinergic Neurons: AcH

2. Peptidergic Neurons: Substance P, VIP, etc.

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23
Q

Sympathetic Ganglia:

A
  1. Celiac
  2. Superior Mesenteric
  3. Inferior Mesenteric
  4. Hypogastric
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24
Q

Sympathetics have short

A

Pre-ganglionic fibers that synapse with ganglion OUTSIDE the layers of the GI wall

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25
Q

Sympathetic post-ganglionic fibers travel to

A

Submucosal or myenteric ganglion, or directly innervate the smooth muscle, endocrine glands, & secretory cells.

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26
Q

Sympathetic Neurotransmitters:

A

Adrenergic Neurons: Norepinephrine

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27
Q

Enteric System

Enteric Ganglion:

A

Located entirely in the submucosal or myenteric plexus on GI tract wall

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28
Q

Enteric System receives sensory information from

A

Mechanoreceptors & chemoreceptors in

mucosa & directly relays to smooth muscle, secretory glands, & endocrine cells as well as other ganglion.

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29
Q

Enteric System receives input from

A

parasympathetic & sympathetic extrinsic systems.

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30
Q

Neurocrines

AcH: location & function

A

from cholinergic neurons –> contraction of muscle wall + relaxation of sphincter + ↑all secretion

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31
Q

Neurocrines

NE: location & function

A

from adrenergic neurons –> relaxation of muscle wall + contraction of sphincter + ↑secretion of saliva

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32
Q

From Neurons of Mucosa or Smooth Muscle

A
  1. Vasoactive intestinal peptide (VIP)
  2. Gastrin-related peptide (GRP)/Bombesin
  3. Enkephalins (opiates)
  4. Neuropeptide Y
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33
Q

Vasoactive intestinal peptide (VIP) –>

A

relaxation of muscle wall + ↑all secretion

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34
Q

Gastrin-related peptide (GRP)/Bombesin –>

A

↑Gastric Secretion

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35
Q

Enkephalins (opiates) –>

A

contraction of smooth muscle + ↓Intestinal Secretion

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36
Q

Neuropeptide Y –>

A

relaxation of smooth muscle + ↓Intestinal Secretion

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37
Q

Gastrointestinal Peptides =

A

Hormones + Paracrines + Neurocrines

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38
Q

Hormones Released from

A

endocrine cells; cells are dispersed throughout GI tract

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39
Q

Hormones Secreted into

A

portal circulation –> liver —> blood stream –> systemic blood

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40
Q

Hormones Blood delivers to

A

Target cells in OR outside of the GI tract

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41
Q

Hormones Must meet following criteria:

A
  1. Secreted from physiologic stimuli & carried via blood to distant site to fulfill physiologic response
  2. Must act independent of neural activity
  3. Must be isolated & chemically ID
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42
Q

Gastrin Hormones:

A

Gastrin-CCK Family

  1. G17 (Little Gastrin):
  2. G34 (Big Gastrin):
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43
Q

G17 (Little Gastrin):

A

↑secretions during/just after meals

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44
Q

2.G34 (Big Gastrin):

A

↑secretions at low levels in between meals

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45
Q

Gastrin Site of Secretion:

A

G (Gastrin) Cells in Stomach Antrum.

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46
Q

Gastrin Stimuli for/against Secretion:

A

Anything to do with Eating

  1. Peptides + Amino Acids: most potent are AA phenylalanine & tryptophan
  2. Distention of Stomach
  3. Vagal Stimulation: occurs via neurocrine GRP acting on G cells
  4. Somatostatin: inhibits secretion
  5. ↓pH: inhibits secretion
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47
Q

Gastrin Action

A
  1. ↑H+ Release by gastric parietal cells

2. ↑Growth of Gastric Mucosa (trophic effect)

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48
Q

Cholecytokinin (CCK) Hormones:

A

Gastrin-CCK Family Act on Two Receptors

  1. CCKA:
  2. CCKB:
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49
Q

CCKA: selective for

A

CCK

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50
Q

CCKB: sensitive for

A

CCK & Gastrin

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51
Q

Cholecytokinin (CCK) Site of Secretion:

A

I Cells in Duodenum & Jejunum

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52
Q

Cholecytokinin (CCK) Stimuli for/against Secretion:

A

Basically the Fat & Protein in a Meal

  1. Monoglycerides + Fatty Acids (NOT TGs)
  2. Small Peptides + AAs
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53
Q

Cholecytokinin (CCK) Action:

A

Functions contribute to Fat, Protein, & CHO Digestion

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54
Q

Cholecytokinin (CCK) cause: Contraction of Gallbladder + Relaxation of Sphincter of Odi:

A

↑Bile into SI

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55
Q

Cholecytokinin (CCK) cause: Secretion of Pancreatic Enzymes:

A

lipases (FA/MG), amylase (CHO), protease

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56
Q

Cholecytokinin (CCK) cause: Secretion of Pancreatic

A

HCO3-

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57
Q

Cholecytokinin (CCK) cause: ↑Growth of Exocrine Pancreas + Gallbladder:

A

tropic effects where CCK acts

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58
Q

Cholecytokinin (CCK) cause: ↓Gastric Emptying = ↑Gastric Emptying Time:

A

↓chyme from stomach –> SI

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59
Q

Secretin Hormones:

A

Secretin-Glucagon Family

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60
Q

Secretin Site of Secretion:

A

S (Secretin Cells) in Duodenum

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61
Q

Secretin Stimuli for/against Secretion:

A

Acidity in Duodenum (pH < 4.5)

  1. ↑H+ In duodenum
  2. ↑FA in duodenum
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62
Q

Secretin Action:

A

Neutralize H+ in Duodenum = protects acid-sensitive pancreatic lipase

  1. ↑Pancreatic HCO3- Secretion
  2. ↑Biliary HCO3- Secretion
  3. ↓Gastrin Effects = ↓H+ secretion from G cells; ↓tropic effects
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63
Q

Glucose-Dependent Insulinotropic Peptide (GIP)

Hormones:

A

Secretin-Glucagon Family

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64
Q

Glucose-Dependent Insulinotropic Peptide (GIP) Site of Secretion:

A

K Cells in Duodenum & Jejunum

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65
Q

Glucose-Dependent Insulinotropic Peptide (GIP) Stimuli for/against Secretion:

A

Only hormone stimulated by all 3 nutrient types

  1. AA
  2. Fatty Acids
  3. Oral Glucose (ORAL ONLY)
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66
Q

Glucose-Dependent Insulinotropic Peptide (GIP) Action:

A
  1. Stimulates Insulin Secretion from Pancreatic β Cells

2. ↓Gastric H+ Secretion

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67
Q

Paracrines Hormones: secreted & act:

A
  • Secreted by endocrine cells
  • Diffuse short distances via ISF or carried via capillaries
  • Act locally within same tissue that secretes them
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68
Q

Paracrines Hormones GI tract:

A

Somatostatin & Histamine

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69
Q

Somatostatin Site of Secretion:

A

D Endocrine + Paracrine Cells

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70
Q

Somatostatin Stimuli for/against Secretion:

A

↓Luminal pH

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71
Q

Somatostatin Action:

A
  1. ↓Secretion of other GI hormones

2. ↓Gastric H+ Secretion

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72
Q

Histamine Site of Secretion:

A

Endocrine-Cells in H+ Secreting Region of Stomach

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73
Q

Histamine Stimuli for/against Secretion:

A

many

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74
Q

Histamine Action:

A

↑Gastric H+ Secretion by Gastric Parietal cells

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75
Q

Neurocrines secreted & act:

A
  • Made by neurons in GI tract
  • Released after action potential
  • Diffuse across synapse to act on target
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76
Q

All contractile muscle is smooth muscle EXCEPT:

A

a) Pharynx
b) ↑1/3 of Esophagus
c) External Anal Sphincter

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77
Q

GI Smooth Muscle =

A

Unitary Smooth Muscle

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78
Q

Cells in Unitary Smooth Muscle are electrically

A

Coupled via gap-junctions that are ↓resistance pathways = fast AP

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79
Q

Unitary Smooth Muscle Fast spread of AP =

A

coordinated + fast muscle contractions

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80
Q

Circular vs. Longitudinal Muscle

A

a) Circular Muscle: contraction shortens a ring of smooth muscle = ↓diameter at a certain segment
b) Longitudinal Muscle: contraction shortens a length of smooth muscle = ↓length of a certain segment

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81
Q

Phasic vs. Tonic Contraction

A

a) Phasic: period contraction then relaxation; found in esophagus, gastric antrum, small intestine = mixing/propelling tissues
b) Tonic: constant low-level contraction without relaxation; found in upper/orad stomach & sphincters (↓esophageal, ileocecal, internal anal sphincter)

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82
Q

orad define:

A

toward the mouth or oral region

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83
Q

Slow Waves:

A

Oscillating Depolarization & Repolarization of Membrane Potential in Gastric Smooth Muscle Cells

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84
Q

Slow Waves: Depolarization Phase:

A

Membrane potential becomes less negative & approaches threshold

a) If depolarization achieves threshold –> burst of APs on top of the slow wave
b) Mechanical response (contraction/tension) lags behind the electrical activity

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85
Q

Slow Waves: Repoalrization Phase:

A

Membrane potential becomes more negative away from threshold

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86
Q

Characteristics of Slow Waves Frequency:

A

Frequency of slow waves determines ==> frequency of APs ==> frequency of contraction

(1) Stomach has slowest frequency (3 slow waves/min)
(2) Duodenum has highest frequency (12 slow waves/min)
(3) Neural input or hormonal input DO NOT affect frequency of slow waves, but DO affect frequency of action potentials

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87
Q

Characteristics of Slow Waves Origin:

A

Interstitial Cells of Cajal

(1) “Pacemaker of GI Smooth Muscle”
(2) Found in myenteric plexus; transmits cyclic depolarization/repolarization to smooth muscle via ↓resistance gap junctions

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88
Q

Characteristics of Slow Waves Mechanism of Slow Wave:

A

(1) Depolarization: Ca++ Channels Open ==> ↑Influx of Ca++ ==> Depolarization
(2) Repolarization: K+ Channels Open ==> ↑Efflux of K+ ==> Repolarization

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89
Q

Characteristics of Slow Waves & Contraction

A

(1) Even the cyclic depolarizations that do not achieve threshold result in weak tonic contraction
(2) Depolarizations that achieve threshold result in phasic contraction
(a) The ↑#APs on top of depolarization ==> ↑Duration of Phasic Contraction

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90
Q

Chewing - Three Functions

A
  1. Mixes food with saliva = wets & lubricates food to allow swallowing
  2. ↓Size of food particles
  3. Mixes CHO with salivary amylase = kicks off CHO digestion
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91
Q

Voluntary vs. Involuntary Chewing

A
  1. Involuntary: sensory information via mechanoreceptors goes to brainstem –> reflex oscillatory chewing
  2. Voluntary: overrides involuntary reflex chewing at any time
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92
Q

Swallowing:

A

Voluntary —> Involuntary

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93
Q

Initiation of swallowing is

A

voluntary in the mouth, then involuntary in the pharynx & beyond

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94
Q

Swallowing Regulated by the

A

swallowing center in the medulla

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95
Q

Sensory information (food in mouth) sensed via

A

somatosensory receptors in pharynx

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96
Q

Information carried to medulla swallowing center via

A

CN IX and X

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97
Q

Medulla sends efferent innervation to

A

striated muscle in the pharynx & ↑1/3 of esophagus

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98
Q

Three Phases of Swallowing:

A
  1. Oral Phase:
  2. Pharyngeal Phase:
  3. Esophageal Phase:
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99
Q

Swallowing Oral Phase:

A

tongue pushes bolus to pharynx, where there are ↑↑↑somatosnesory receptors

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100
Q

Swallowing Pharyngeal Phase:

A

propel food through pharynx to esophagus in the following order:
• Soft palate pulls upward to prevent reflux into nasopharynx
• Epiglottis close opening of larynx (∴breathing inhibited during pharyngeal phase)
• Upper esophageal sphincter relaxes creating an opening for food into esophagus
• Peristaltic wave is initiated

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101
Q

Swallowing Esophageal Phase:

A

overlaps with esophageal motility

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102
Q

Esophageal Motility: Upper esophageal sphincter opens during

A

the pharyngeal phase of swallowing
• Bolus of food moves from pharynx to esophagus
• Upper esophageal sphincter closes to prevent reflux into pharynx

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103
Q

Esophageal Motility Primary Peristaltic Contraction:

A

mediated by swallowing reflex

• Series of coordinated sequential contractions that generate pressure just behind bolus, pushing it along

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104
Q

Esophageal Motility Food Approaches Lower Esophageal Sphincter - Three Things Happen

A
  • Lower esophageal sphincter opens from vagal nerve release of VIP (Vasovagal Reflex)
  • Orad region of stomach relaxes; ↓P_orad allows bolus in stomach (“Receptive Relaxation”)
  • Lower esophageal sphincter closes P_Sphincter > P_Orad or P_Esophageal
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105
Q

Esophageal Motility Secondary Peristaltic Contraction -

A

back up to primary peristaltic contraction via enteric system
• If primary peristaltic contraction doesn’t clear food, secondary peristaltic contraction begins

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106
Q

Esophageal Motility Pressure & the Esophagus:

A
  • Recall, P_intrathoracic is negative ===> P_Esophageal is also negative
  • P_abdomen > P_Esophagus
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107
Q

Esophageal Motility: Two consequences of negative intra-esophageal pressure, explaining purpose of esophageal sphincters

A
  1. Air can enter the esophagus ==> Upper Esophageal Sphincter prevents this
  2. Gastric contents can enter the esophagus ==> Lower Esophageal sphincter prevents this
    * ***In obesity or pregnancy, P_abdomen > P_Lower_Esophageal_Sphincter = GERD
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108
Q

Gastric Motility Muscles of Stomach:

A

outer longitudinal layer –> middle circular layer –> inner oblique layer
• ↑Thickness of muscle wall from proximal to distal end of stomach

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109
Q

Gastric Motility Structural Organization:

A

Fundus + Body + Antrum

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110
Q

Gastric Motility Orad =

A

fundus + proximal portion of body –> thin walled for weaker contractions

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111
Q

Gastric Motility Caudad =

A

distal body + antrum –> thick walled for stronger contractions to mix & propel food

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112
Q

Gastric Motility Innervation

A
  • Extrinsic Parasympathetic + Sympathetic Innervation

* Intrinsic Enteric Innervation from Myenteric & Submucosal Plexuses

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113
Q

Gastric Motility Three Phases:

A
  1. Receptive Relaxation
  2. Mixing & Digestion
  3. Gastric Emptying
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114
Q

Gastric Motility Receptive Relaxation -

A

Orad Territory
• Function of orad region is receive bolus by relaxing when lower esophageal sphincter distends
• Relaxation of orad region = ↓P_Orad = ↑V_Orad = bolus can enter stomach

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115
Q

Gastric Motility Mixing & Digestion -

A

Caudad Territory
• Contractions around mid-/distal-body break down bolus (chyme), mix gastric contents, & propel food
• ↑Strength of contractions distally also close pylorus —> chyme pushed back into stomach (“Retropulsion”)

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116
Q

Gastric Motility Parasympathetic stimulation & gastrin/motilin =

A

↑frequency of APs & contraction force (x slow waves)

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117
Q

Gastric Motility Sympathetic stimulation & secretin/GIP =

A

↓frequency of APs & contraction force (not slow waves)

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118
Q

Gastric Motility Gastric Emptying -

A

Monitored to ensure appropriate size ( slows gastric emptying –> ↑time for absorption of fatty gastric contents
• ↑H+ = ↑enteric reflex –> myenteric plexus slows gastric emptying –> ↑time for HCO3- neutralization

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119
Q

Throughout stomach & small intestine, migrating myoelectric complexes are

A

Mediated by motilin. These are periodic contractions (every 90 mins) during fasting that clear stomach & SI of residual food/chyme contents.

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120
Q

Small Intestine Motility

Innervation:

A
  1. Parasympathetic Innervation (Vagus Nerve): ↑contraction of intestinal smooth muscle
  2. Sympathetic Innervation (Celiac + Superior Mesenteric Ganglion): ↓contraction of intestinal smooth muscle
121
Q

Small Intestine Motility Segmentation & Peristaltic Contractions ~ Coordinated by

A

Enteric System

122
Q

Small Intestine Motility Segmentation Contractions =

A

MIX CHYME
• Contraction occurs within a bolus of chyme
• Bolus of chyme is split, some sent in the orad direction & in the caudad direction
• Back/forth movement mixes chyme, no propulsion

123
Q

Small Intestine Motility Peristaltic Contractions =

A

PROPEL CHYME
• Contraction occurs behind bolus of chyme & relaxation occurs in front of bolus of chyme
• Chyme is propelled forward
• Simultaneous contraction/relaxation is regulated by parasympathetic/sympathetic innervation respectively

124
Q

Small Intestine Motility Vomiting ~ Regulated by

A

Vomiting Center in Medulla

125
Q

Small Intestine Motility Vomiting Sensory innervation:

A

Vestibular system, back of throat, GI tract, & chemoreceptors in 4th ventricle

126
Q

Small Intestine Motility Vomiting Motor innervation:

A

↑reverse peristalsis beginning at SI –> relaxation of stomach & lower esophageal
sphincter –> inspiration to generate ↑P_Abdominal –> YAK!

127
Q

Large Intestine Motility Overview:

A
  • Material not absorbed in SI is sent to LI, where it is called feces
  • SI contents pass through the ileocecal valve, followed by contraction of the ileocececal sphincter
  • Prevents reflux into SI
128
Q

Large Intestine Motility Segmentation Contractions:

A
  1. As in SI, segmentation contractions occur in the middle of a bolus of feces to mix contents
  2. Mediated by haustra
129
Q

Large Intestine Motility Mass Movements:

A

~ 1-3/day

  1. Function to move contents of LI over long distances
  2. As mass movements occur, water absorption occurs in the distal colon; contents become more difficult to move as feces approaches rectum
130
Q

Large Intestine Motility: Defecation: As rectum enlarges with entering feces

A

smooth muscle of rectum contracts & internal anal sphincter relaxes (“Rectosphincteric Reflex”)

131
Q

Large Intestine Motility Defecation: Defecation requires that the

A

external anal sphincter also relaxes; this occurs when rectum is 25% full

132
Q

Large Intestine Motility Defecation: When appropriate, external anal sphincter relaxes & smooth muscle in anal canal contracts =

A

defecation

133
Q

Large Intestine Motility Gastrocolic Reflex: Distention of stomach by food =

A

↑Motility of Colon + ↑Frequency of Mass Movements

134
Q

Large Intestine Motility Gastrocolic Reflex:

Afferent limb:

A

mediated by parasympathetics in stomach

135
Q

Large Intestine Motility Gastrocolic Reflex:

Efferent limb:

A

mediated by hormones CCK & gastrin

136
Q

Salivary Secretions ~

A

1 Liter/Day

137
Q

Structure of Parotid Glands:

A

serous cells secreting aqueous fluid (=water, ions & enzymes)

138
Q

Structure of Submandibular & Sublingual Glands:

A

serous AND mucous cells secreting aqueous

fluid AND mucin glycoproteins

139
Q

Acinus:

A

Cluster of Grapes of Glands = Cluster of Acinus

140
Q

Acinus: blind end of duct lined with

A

acinar cells where saliva is produced

141
Q

Saliva from acinus through

A

short intercalated duct lined with myoepithelial cells

142
Q

Myoepithelial cells neuronal stimulation –>

A

contraction / ejection of saliva

143
Q

Saliva then passes through striated duct lined with

A

ductal cells

144
Q

Ductal cells alter the

A

electrolyte composition of the saliva

145
Q

Both parasympathetic & sympathetic stimulation =

A

↑Saliva Production (Parasympathetic > Sympathetic)

146
Q

Effect of Flow Rate on Saliva Composition:

↑Flow Rate =

A

↓Contact time original saliva has with ductal cells =

↓absorption / ↓secretion = isotonic saliva ~ plasma

147
Q

Effect of Flow Rate on Saliva Composition

↓Flow Rate =

A

↑Contact time original saliva has with ductal cells =

↑absorption / ↑secretion = hypotonic saliva

148
Q

Effect of Flow Rate on Saliva Composition

EXCEPTION =

A

HCO3-

(1) Bicarbonate: ↑concentration should follow ↓flow rate
(2) Bicarbonate secretion is selectively stimulated only when saliva production is stimulated; it is more dependent on para/sympa innervation for saliva production than flow
(3) ∴↑[Bicarbonate] in saliva with ↑Flow Rate

149
Q

Regulation of Salivary Secretion is

A

Salivary secretion is only neuronal control; no hormonal control

150
Q

Regulation of Salivary Secretion Parasympathetic Input:

A

CNVII & CN IX

(1) Postganglionic fibers release AcH which bind to M-receptors gland cell
(2) M-Receptor activation = ↑IP3/Ca++
(3) ↑IP3/Ca++ = ↑Secretion
(4) ↑Para stimulation with conditioning, food, smell, nausea
(5) ↓Para stimulation with dehydration, fever, sleep

151
Q

Regulation of Salivary Secretion Sympathetic Input:

A

T1-T3 & Superior Cervical Ganglion

(1) Postganglionic fibers release NE; bind to β-receptors
(2) ↑β-Receptor activation = ↑cAMP = ↑Secretion

152
Q

Regulation of Salivary Secretion Net Effect of Parasympathetic & Sympathetic Input

A

(1) ↑Saliva Production
(2) ↑HCO3- Secretion (Selectively Secreted!)
(3) ↑Enzyme Secretion
(4) Contraction of Myoepithelial Cells

153
Q

Gastric Juice ~

A

HCl, Pepsinogen, Intrinsic Factor & Mucus

154
Q

Body: Cell Types

A 
Parietal Cells (Oxyntic)
Chief Cells (Peptic)
155
Q

Antrum: Cell Types

A

G Cells

Mucosal Neck Cells

156
Q

Parietal Cells (Oxyntic) Secretions:

A

HCl + Intrinsic Factor

157
Q

Chief Cells (Peptic) Secretions

A

Pepsinogen

158
Q

G Cells Secretions

159
Q

Mucosal Neck Cells Secretions

A

Mucus, HCO3-, Pepsinogen

160
Q

HCl Secretion ~

A

Parietal Cell’s Function to Acidify Gastric Contents to pH ~ 1-2

161
Q

↓pH functions to convert inactive

A

pepsinogen (made by chief cells in body of stomach) –> active pepsin (protease for proteins)

162
Q

Gastric parietal cells’ cellular mechanism based on structure of

A

luminal/apical & basolateral membranes

(1) Luminal Membrane: H+/K+ ATPase + Cl- Channel
(2) Basolateral Membrane: Na+/K+ ATPase + Cl-/HCO3- Exchanger
(3) Cell contains carbonic anhydrase

163
Q

Cellular Mechanism ~ Net HCl secretion + HCO3- absorption

A

(1)CO2 produced by aerobic metabolism combines with H2O –> H2CO3 –> H+ + HCO3-
(2)H+ is secreted into the lumen against its’ gradient via the apical membrane H+/K+ ATPase
(a)H+/K+ ATPase or H+ secretion is the target of PPI (Omeprazole)
(3)Cl- follows H+ via diffusion through Cl- channel ==> HCl secretion into lumen is complete
(4)HCO3- is absorbed into blood stream via basolateral Cl-/HCO3- exchanger ==> HCO3-
absorption is complete
(a)↑pH just after meal occurs because of the ↑HCO3- absorption

164
Q

Regulation of HCl Secretion

A

(1) AcH = Neurocrine
(2) Histamine = Paracrine
(3) Gastrin = Hormone

165
Q

Regulation of HCl Secretion

AcH = Neurocrine

A

(a) ↑AcH –> ↑M3 Activation on Parietal Cells –> ↑DAG + IP3 –> ↑Ca++ –> ↑H+ Secretion by Parietal Cells
(b) Blocked by atropine

166
Q

Regulation of HCl Secretion

Histamine = Paracrine

A

(a)↑Histamine from Enterochromaffin Like Cells (ELC) –> ↑H2
Receptors –> ↑Gs-PCR –> ↑cAMP –> ↑H+ Secretion
(b)Blocked by cimetidine

167
Q

Regulation of HCl Secretion

Gastrin = Hormone

A

(a)↑Gastrin from G Cells in Antrum –> ↑Gastrin in Systemic Blood –> ↑Gastrin to CCKB –> ↑IP3/Ca++ –> ↑H+

168
Q

Regulation of HCl Secretion

Interaction of AcH, Histamine & Gastrin

A

(i) Rate of H+ secretion is regulated by each but also from their interactions = “Potentiation”
(ii) ↑H+ Secretion b/c the stimulants act on different receptors & in some cases via different 2nd messengers
(iii) ↑H+ Secretion b/c atropine & gastrin activate ECL cells –> ↑Histamine Release via 2nd mechanism

169
Q

Stimulation of H+ Secretion:

Vagus nerve innervates gastric parietal cells & G cells in antrum of stomach directly, but

A

by different nuerotransmitters

170
Q

Stimulation of H+ Secretion:

Vagus nerve –> parietal cells –>

A

AcH release –> HCl Secretion

171
Q

Stimulation of H+ Secretion:

Vagus nerve –> G cells –>

A

GRP release –> Gastrin Secretion –> Blood –>

Parietal Cells –> H+ Secretion

172
Q

Stimulation of H+ Secretion:

Consequence of Atropine?

A

Atropine will block the direct effects of AcH on parietal cells, but will not block the indirect effects of vagus nerve on G cells, as this neurotransmitter is different (GRP)

173
Q

Three Phases of Gastric HCl Secretion:

A

Cephalic, Gastric & Intestinal

174
Q

Phases of Gastric HCl Secretion:

Cephalic (30%) Stimuli:

A
  1. Smell
  2. Taste
  3. Conditioning
175
Q

Phases of Gastric HCl Secretion:

Cephalic (30%) Mechanism:

A
  1. Vagus Nerve –> Direct Innervation of Parietal Cells (AcH)–> HCl Secretion
  2. Vagus Nerve –> Direct Innervation of G Cells (GRP)–> Gastrin –> Indirect HCl Secretion
176
Q

Phases of Gastric HCl Secretion:

Gastric (60%) Stimuli: Distention of Stomach

A

Mechanism:

  1. Vagus Nerve –> Direct Innervation of Parietal Cells (AcH)–> HCl Secretion
  2. Vagus Nerve –> Direct Innervation of G Cells (GRP)–> Gastrin –> Indirect HCl Secretion
177
Q

Phases of Gastric HCl Secretion:

Gastric (60%) Stimuli: Distention of Antrum

A

Mechanism:

Distention of antrum –> local reflex stimulation of gastrin –> indirect HCl secretion

178
Q

Phases of Gastric HCl Secretion:
Gastric (60%) Stimuli:
1. AA & Small Peptides
2. Caffeine/Alcohol

A

Mechanism:

Direct AA & Small Peptide stimulation of gastrin –> indirect HCl secretion

179
Q

Phases of Gastric HCl Secretion:

Intestinal (10%) Stimuli/Mechanism:

A

Products of protein digestion

180
Q

Inhibition of H+ Secretion:

Movement of Chyme Into SI (↓pH)

A

(a) When chyme moves to SI, pepsinogen activation via ↓pH is no longer needed; HCl secretion needs to be inhibited
(b) Loss of foodstuffs/chyme = loss of H+ buffer = relative excess of H+ = ↓pH
(c) ↓pH –> ↓gastrin release –> indirect ↓parietal cell H+ secretion

181
Q

Inhibition of H+ Secretion:

Somatostatin

A

(a) Direct Pathway: somatostatin + Gi-PCR Parietal Cell Receptors –> ↓AC –> ↓cAMP –> ↓H+ Secretions
(b) Indirect Pathway: somatostatin –> ↓ECL Histamine Release + ↓G Cell Gastrin Release –> ↓H+ Secretions

182
Q

Inhibition of H+ Secretion:

Prostaglandins

A

PGs –> ↓Gi-PCR Parietal Cell Receptors –>

↓AC –> ↓cAMP –> ↓H+ Secretions

183
Q

Review of Protective Mechanisms to prevent Peptic Ulcer Disease (PUD)

A
  1. Mucus: secreted by mucous neck glands,
    forming protective gel like layer
  2. HCO3-: secreted by parietal cells, trapped
    in mucous, neutralizes H+ & pepsin (requires ↓pH for activity)
  3. PGs: inhibit release of H+ by antagonizing
    cAMP (histamine) pathway
  4. Growth Factors / Blood Flow
184
Q

Review of Potentially Damaging Mechanisms Peptic Ulcer Disease (PUD)

A

Review of Potentially Damaging Mechanisms

  1. Excess H+
  2. Pepsin
  3. Helicobacter Pylori Infection
  4. NSAIDS (anti-PGs)
  5. Stress, Smoking, Alcohol
185
Q

Gastric Ulcers

Defect:

A

Mucosal Barrier

H+ & pepsin can digest protective mucosa

186
Q

Gastric Ulcers

Etiology & Pathogenesis

A
  1. H. Pylori colonizes gastric mucosa because it
    secretes urease which ↑pH surrounding pH
  2. H. Pylori attaches to parietal cells –> ↑cytokines
  3. ↑Cytokines –> Damage to Parietal Cells
187
Q

Gastric Ulcers

H+ & Gastrin Secretions

A
  1. ↓H+ Secretion b/c H+ gets in damages mucosa

2. ↑Gastrin Secretion b/c ↓H+ Secretion

188
Q

Gastric Ulcers

Diagnosed:

A 
Diagnosed with CO2 breath test post-ingestion
of urea (converted to CO2+NH3 via urease)
189
Q

Duodenal Ulcers

Defect:

A

↑H+ Secretions

190
Q

Duodenal Ulcers

Etiology and Pathogenesis:

A

1.H. Pylori colonizes gastric mucosa & indirect effect is ↓somatostatin secretion
2. ↓Somatostatin = ↓inhibition of G cells –> ↑Gastrin Secretion –> ↑H+ secretion to inhibit excess Gastrin
3.H. Pylori spreads to duodenum –> ↓HCO3- from
pancreatic secretions
4.Overall, ↑H+ of Duodenum & ↑Mass of Parietal Cells (Trophic Effects)

191
Q

Duodenal Ulcers

H+ & Gastrin Secretions

A
  1. ↑Gastrin Secretion

2. ↑H+ Secretions

192
Q

Zollinger-Ellison Syndrome (Gastrinoma)

Defect:

A

↑↑↑Gastrin Secretions (Pancreatic Tumor)

193
Q

Zollinger-Ellison Syndrome (Gastrinoma)

Etiology & Pathogenesis:

A
  1. Pancreatic tumor secretes excess gastrin
  2. ↑Gastrin –> ↑H+ and ↑Parietal Mass
  3. ↑Gastrin –> ↓pH of duodenum –> ulcer +
    inactivation of pancreatic lipases
  4. ↓Lipase activity –> steatorrhea
    5.Gastrin not feedback inhibited (neoplasia)
194
Q

Zollinger-Ellison Syndrome (Gastrinoma)

H+ & Gastrin Secretions:

A
  1. ↑Gastrin Secretion

2. ↑H+ Secretions

195
Q

Gastric Ulcers, Duodenal Ulcers, & Zollinger-Ellison Syndrome (Gastrinoma):
Treatment:

A

Tx w/Cimetidine and Omeprazole

196
Q

Pepsinogen Secretion

A

Recall, pepsinogen is secreted by chief cells & mucous cells in oxyntic glands & is activated by ↓pH to digest proteins

197
Q

Pepsinogen Secretion

Stimuli for Pepsinogen Secretion:

A

(1) Vagal Stimulation
(2) H+ Secretion –> ↑Local Reflex –> ↑Chief Cell Stimulation –> ↑Pepsin Release
This ensures that pepsinogen will only be secreted when the pH is low enough to activate it to pepsin

198
Q

Intrinsic Factor Secretion

A
  1. Mucoprotein secreted by gastric parietal cells require for B12 absorption in the ileum
  2. Deficiency of IF –> Pernicious Anemia
199
Q

Pancreatic Secretions:

A

~ HCO3- & Enzymatic Components

200
Q

Structure of Pancreatic Exocrine Glands:

Acinus:

A

Blind end branching duct lined with acinar cells responsible for the enzymatic component of pancreatic secretions

201
Q

Structure of Pancreatic Exocrine Glands:

Ductal Cells:

A

Epithelium that line the ducts; has specialized extension into acinus called centroacinar cells

202
Q

Structure of Pancreatic Exocrine Glands:

Centroacinar Cells:

A

Responsible for the HCO3- component of pancreatic secretions

203
Q

Innervation of Exocrine Pancreas

Sympathetic Innervation =

A

↓Pancreatic Secretion

(1) Sympathetic innervation from post-ganglionic nerves from celiac & superior mesenteric plexues

204
Q

Innervation of Exocrine Pancreas

Parasympathetic Innervation =

A

↑Pancreatic Secretion
(1) Parasympathetic innervation from vagus nerve preganglionic –> synapse in enteric system –> synapse in exocrine tissue

205
Q 
Formation of Pancreatic Secretion
Enzymatic Component (Acinar Cells):
A

(1) Enzymatic components includes amylases & lipases (secreted as active enzymes) or proteases (need activation)
(2) Made in the RER of Acinar Cells –> Golgi Apparatus –> Packaged as Zymogens –> Stored Until Stimulus Arrives

206
Q

Formation of Pancreatic Secretion
HCO3- Aqueous Component
(Centroacinar / Ductal Cells)
Centroacinar

A

(1) Aqueous component is isotonic solution of Na+, Cl-, K+ & HCO3-
(2) Centroacinar cells secrete initial isotonic component & ductal cell transporters modify component
(a) Apical Transporters: Cl-/HCO3- Exchanger
(b) Basolateral Membrane: Na+/K+ ATPase & Na+/H+ Exchangers

207
Q

Formation of Pancreatic Secretion
HCO3- Aqueous Component
(Centroacinar / Ductal Cells)
Ductal Cells

A

(1) Ductal cell Carbonic Anhydrase combines CO2 + H2O –> H2CO3 –> H+ + HCO3-
(a) HCO3- is secreted into pancreatic juice (lumen) via apical transporter & H+ is absorbed into the blood
(2) Net Result: HCO3- secreted into pancreatic ductal juice & H+ acidifies pancreatic venous blood
(a) Note how this is opposite (balances!) the HCl secreting parietal cells of the stomach

208
Q

Δ Pancreatic Flow Rates yield changes in

A

ΔPancreatic Flow Rates yield changes in HCO3- & Cl concentrations, but not Na+ and K+

209
Q

Δ Pancreatic Flow Rates Unlike the relationship for the salivary glands

A

(a)↓Flow Rate = ↓HCO3- and ↓Cl-
(b)↑Flow Rate = ↑HCO3- and ↑Cl-
Explanation:
(a)At ↓rates of secretion, secretion is Na+ & Cl-
(b)At ↑rates of secretion, secretion is Na+ & HCO3-

210
Q

Regulation of Pancreatic Secretion
Acinar Cells ~ Enzymatic Secretion
CCK From I-Cells

A
  1. Stimulated by AA, peptides & FA in SI lumen
    • AA phenylalanine, methionine & tryptophan
    are most potent stimuli for CCK secretion
  2. CCK acts via IP3/Ca++ signaling pathway –>
    ↑Secretions
211
Q

Regulation of Pancreatic Secretion
Acinar Cells ~ Enzymatic Secretion
AcH

A
  1. Stimulates AcH muscarinic receptors on the
    pancreatic acinar cells
  2. Potentiates CCK action via vasovagal reflex
212
Q

Regulation of Pancreatic Secretion
Ductal Cells ~ Aqueous Secretion
Secretin From Duodenal S-Cells

A
  1. Secreted in response to ↑H+ in chyme from
    stomach (=↓pH)
  2. Stimulates ↑HCO3- secretion from pancreas
  3. Ensures activity of ↑pH-requiring pancreatic
    lipases
213
Q

Regulation of Pancreatic Secretion
Ductal Cells ~ Aqueous Secretion
CCK

A

Potentiates secretin effects

214
Q

Regulation of Pancreatic Secretion
Ductal Cells ~ Aqueous Secretion
AcH

A

Potentiates secretin effects

215
Q

Three Phases of Pancreatic Secretion

A
  1. Cephalic Phase:
  2. Gastric Phase:
  3. Intestinal Phase:
216
Q

Pancreatic Secretion

Cephalic Phase:

A

Initiated by smell, taste & conditioning via Vagus Nerve; enzymatic component

217
Q

Pancreatic Secretion

Gastric Phase:

A

Initiated by distention of stomach via Vagus Nerve; enzymatic component

218
Q

Pancreatic Secretion

Intestinal Phase:

A

Important (80% of secretion); enzymatic & aqueous components are secreted

219
Q

Circuit of Biliary System Step 1:

A

Hepatocytes constantly synthesize & secrete bile

220
Q

Circuit of Biliary System Step 2:

A

Bile flows from liver via bile ducts to fill gallbladder, where it is stored
• Gallbladder concentrates bile via H2O & ion absorption

221
Q

Circuit of Biliary System Step 3:

A

Stored bile flows into lumen of duodenum
• Chyme in duodenum –> ↑CCK release –> contraction of gallbladder + relaxation of
sphincter of ODI
• Bile emulsifies & solubilizes the water-insoluble dietary lipids

222
Q

Circuit of Biliary System Step 4:

A

Post-lipid absorption, bile is recycled via enterohepatic circulation (portal blood)
• Ileum: Na+/Bile Salt cotransporter reabsorbs bile into the portal blood; important this occurs in ileum; bile salts around for lipid metabolism for entire length of SI!
• Portal blood takes bile salts back to hepatocytes for extraction

223
Q

Circuit of Biliary System Step 5:

A

Bile from the portal circulation is extracted by the hepatocytes
• Only small amount of bile salts are excreted in the feces (600 mg/day of 2.5 g total)
• Enzyme for bile (cholesterol 7α-Hydroxylase) is inhibited by bile salts coming back
• ↑Bile salts from portal –> ↑Biliary Secretion of Bile Salts (“Choleretic Effect)

224
Q

Composition of Bile ~

A

Bile Salts (50%) + Phospholipids (40%) + Cholesterol (4%) + Bilirubin (2%) + Ions/Water

225
Q

Bile Salts: Represent Modification of Two Primary Bile Acids

A

Primary Bile Acids:

Cholic Acid + Chenodeoxycholic Acid

226
Q

Bile Salts: Secondary Bile Acids:

A

Deoxycholic Acid + Lithocholic Acid

227
Q

Secondary bile acids are converted from primary bile acids via

A

intestinal bacteria post-release into SI

228
Q

Bile Salts: Liver conjugates bile acids (cholic, deoxycholic, chenodeoxycholic & lithocholic acids) with taurine or glycine to form

A

eight distinct bile salts

229
Q

Pre-conjugation, the pK of these bile salts

230
Q

Duodenal pH ~ 3-5, thus pre-conjugation bile acids (primary or secondary) would be in the

A

non-ionized (and therefore insoluble) form

231
Q

Post-conjugation, the pK of these bile salts ~1-4; now they can exist in

A

ionized form in the duodenum & succesfully

emulsify lipids for absorption & digestion as micelles (+ due to amphipathic properties)

232
Q

Phospholipids & Cholesterol - included in micelles & (the phospholipids) help package

A

lipids in micelles

233
Q

Bilirubin

A

~ Yellow-colored Pigment

234
Q

RES metabolizes hemoglobin –>

A

bilirubin –> liver metabolizes bilirubin via glucuronidation –> bilirubin glucuronide

235
Q

Bilirubin Glucuronide =

A

Conjugated Bilirubin = Yellow Pigment

236
Q

Conjugated Bilirubin –>

A

secreted into intestine –> converted to urobilinogen via intestinal bacteria

237
Q

Urobilinogen –>

A

Urobilin & Sterobilin (Dark Color in Stool)

238
Q

Absorption (villi-mediated) can occur by two mechanisms:

A

cellular (substance crosses both apical & basolateral membranes) OR paracellular
(substance cross tight junctions in between cells into blood)

239
Q

Everything is absorbed in the small intestine except

A

Vitamin B12 & Bile Salts, which are absorbed in the ileum

240
Q

All CHO broken down into

A

glucose, galactose, fructose

241
Q

Disaccharides

A 
1. Trehalose-->2xGlucose
• Enzyme: Trehalase
2. Lactose-->Glucose+Galactose
• Enzyme: Lactase
3. Sucrose-->Glucose+Fructose
• Enzyme: Sucrase
242
Q

Sucrase:

A

the hydrolysis of sucrose to fructose & glucose

243
Q

α-Amylase:

A

linear α(1,4) glycosidic linkages, makes maltose

244
Q

α-Dextrinsase:

A

Hydrolysis of (1->6)-alpha-D-glucosidic linkages

245
Q

Maltase:

A

only alpha form of the maltose to glucose.

246
Q

Glucose & Galactose

Apical Membrane:

A
  • Absorbed via Na+/Glucose SGLT1 Cotransporter

* Occurs against electrochemical gradient, driven by basolateral Na+/K+ ATPase

247
Q

Glucose & Galactose

Basolateral Membrane:

A

Facilitated diffusion via GLUT2

248
Q

Fructose

Apical Membrane:

A

Absorbed via GLUT5,

249
Q

Fructose

Basolateral Membrane:

A

Facilitated diffusion via GLUT2

250
Q

Lactose Intolerance

A
  • Failure to break down lactose into monosaccharides from lactase deficiency
  • Lactose is non-absorbable & holds water in the lumen –> osmotic diarrhea
251
Q

All protein broken down into

A

AA, dipeptides & tripeptides via proteases in stomach & SI

252
Q

Stomach: Pepsin activated from pepsinogen by

A

↓pH; inactivated in duodenum by pancreatic aqueous (HCO3-) secretions

253
Q

SI Enterokinase (BB enzyme) activates

A

trypsinogen–>trypsin

254
Q

SI Trypsin activates the others:

A
  • Chymotrypsinogen->Chymotrypsin
  • Proelastase->Elastase
  • Procarboxypeptidase A/B -> Carboxypeptidase A/B
  • Auto-activates more of itself: Trypsinogen->Trypsin
255
Q

Unlike CHO, protein can be

A

absorbed as larger molecules

256
Q

L-Amino Acids

Apical Membrane:

A
  • Absorbed via Na+/AA Cotransporter

* Powered via Na+/K+ ATPase

257
Q

L-Amino Acids

Basolateral Membrane:

A
  • Facilitated diffusion

* On both apical/basolateral side there are separate transporters for acidic, basic, neutral, imino AA

258
Q

Dipeptides & Tripeptides

Apical Membrane:

A
  • Absorbed via H+/Di-Tripeptide Cotransporter
  • Powered by Na+/H+ apical cotransporter
  • Majority hydrolyzed by peptidase
259
Q

Dipeptides & Tripeptides

Basolateral Membrane:

A
  • AA via facilitate diffusion

* Peptides absorbed unchanged

260
Q

Chronic Pancreatitis / CF proteins:

A
  • Deficiency of all pancreatic enzymes (more than proteases)
  • Even if trypsin alone was lost, all proteases would be inactive
  • Recall that role of pepsin in protein digestion (stomach) is not required
261
Q

Cystinuria proteins:

A
  • Genetic deficiency in apical transporter for cystine, ornithine, arginine, lysine in SI & kidney
  • Excess cystine excreted in urine (cystinuria) & feces
262
Q

Lipids Stomach start digestion:

A

• Lingual & gastric lipases start lipid digestion
-> MG + 2xFA
• CCK-mediated slowing of gastric emptying; ↑pancreatic digestion
• Lipids emulsified here by dietary protein (no bile salts in stomach)

263
Q

Lipids Small Intestine digestion:

A
  1. Bile salts emulsify lipids
  2. Pancreatic enzymes:
    • Pancreatic Lipase: MG + 2xFA
    • Cholesterol Ester Hydrolase:
    Cholesterol + FAs
    • PLA2: Lysolecithin + FA
    • Colipase: prevents bile-salt inactivation of pancreatic lipase
264
Q

Lipids Products of Digestion

A

1.MGs + FAs - insoluble
2.Cholesterol - insoluble
3. Lysolecithin - insoluble
4.Glycerol - soluble
• Thus, micelles are needed to solubilize products for transport

265
Q

Lipids Disorders

Pancreatic Insufficiency

A

• ↓Lipid digesting enzymes
• ↓HCO3- secreted by pancreas;
lipid digesting enzymes inactivated at ↓pH

266
Q

Lipids Disorders

Acidity of Duodenum:

A

↑H+ (ZE Syndrome) inactivates lipid digesting enzymes

267
Q

Lipids Disorders

Deficiency of Bile Salts:

A

No solubilizing lipids; liver failure of ileal resection

268
Q

Lipids Disorders

Bacterial Overgrowth:

A

Bacteria convert bile salts -> bile acids (non-ionized form)

269
Q

Lipids Disorders

Decreased Intestinal Cells:

A

Tropical sprue: ↓Surface Area

270
Q

Lipids Disorders

Abetalipoproteineima

271
Q

Vitamins Fat Soluble

A

(A, D, E and K)

272
Q

Vitamins Water Soluble

A

(B1, B2, B6, C, Biotin, Folic Acid, Nicotinic Acid,

Pantothenic Acid)

273
Q

Vitamin B12 Cleaved from

A

food in stomach by actions of pepsin

274
Q

Vitamins Absorption Fat Soluble:

A

same as lipids

275
Q

Vitamins Absorption Water Soluble:

A

Na+-Cotransporter

276
Q

Vitamins Absorption Vitamin B12:

A
  1. Cleaved B12 (stomach) binds RProteins made in saliva
  2. SI: pancreatic lipases degrade RProtein, allowing B12 to bind IF secreted by parietal cells
  3. Absorbed in ileum
277
Q

Vitamins Disorder

Pernicious Anemia

A

May follow gastrectomy (loss of IF) or ileal resection

278
Q

Calcium Digestion

A

Cleaved from food in stomach & Small Intestine

279
Q

Calcium Absorption

A
  • Absorption mediated by 1-25 Dihydroxycholecalficerol (Vit D)
  • Vit D –> ↑calbindin D-28K = Cabinding protein in SI
  • Vit D synthesized in liver & renal tubules (1α-Hydroxylase)
280
Q

Calcium Disorders

Rickets & Osteomalacia:

A

Can occur with renal failure –> ↓1α-Hydroxylase –> ↓Vit D –> ↓Calbinding D-28K –> ↓Ca++

281
Q

Fluids & Volumes in the GI Tract

Total Volume of Fluid:

A

~ 9L = 2L Dietary Fluids + 7L GI Secretions

282
Q

Fluids & Volumes in the GI Tract

Majority is absorbed by

A

epithelial cells; 100-200 mL is excreted in feces

283
Q

Fluids & Volumes in the GI Tract

Disruption of absorption –>

284
Q

Fluids & Volumes in the GI Tract:

In addition to absorbed fluid, the epithelial cells also

A

secrete some fluid

285
Q

Fluids & Volumes in the GI Tract:

Both absorption & secretion can occur

A

transcellularly or paracellularly; depends on presence or °leakiness of tight junctions

286
Q

Villi-mediated absorption is always

A

isoosmotic; solute & water absorption occur simultaneously

287
Q

Absorption Jejunum ~

A

Net Absorption of NaHCO3

288
Q

Absorption Jejunum

Apical Membrane:

A

Na+ absorbed via Na-Coupled Transporters (Na/Glucose; Na/AA; Na/H)

289
Q

Absorption Jejunum

Basolateral Membrane:

A

Na+/K+ ATPase (also involved in nutrient absorption) completes absorption

290
Q

Jejunum Note H+ & HCO3- for Na/H apical cotransporter come from

A

H2O+CO2; H+ secreted via Na/H; HCO3- absorbed into blood –> ∴Net NaHCO3 absorption

291
Q

Ileum ~

A

Net Absorption of NaCl
• HCO3- from CA-mediated action (in jejunum) is absorbed in the blood
• In Ileum, it is secreted into lumen by Cl-/HCO3- apical transporter –> ∴ Net NaCl absorption

292
Q

Colon ~

A

Na Absorption & K Secretion
• Aldosterone mediated synthesis of Na+ channels –> ↑Na Absorption
• ↑Na+ entry into epithelial cell –> ↑activity of basolateral Na/K ATPase –> ↑K+ into cell –>
↑K Secretion
• K+ secretion is flow-rate dependent; ↑intestinal flow rate = ↑K+ Secretion = Hypokalemia

293
Q

Epithelium lining crypts secrete fluid & electrolytes; different from

A

villi which mainly absorb

294
Q

Cholera Mechanism:

A
  • Normally, ions & H2O secreted by crypts are reabsorbed by the villi
  • Cholera toxin A subunit detaches & catalyzes ADP ribosylation of α subunit of Gs protein coupled to AC
  • ADP ribosylation inhibits GTPase activity of α subunit, inhibiting GTP –> GDP conversion –> ↑↑↑AC
  • ↑↑↑AC –> ↑↑↑cAMP –> Excessive Secretion –> Secretory Diarrhea
295
Q

Diarrhea Compensation Mechanism:

A
  • Diarrhea –> ↓ECF –> ↓Arterial Pressure –> RAAS will attempt to correct
  • Diarrhea –> ↓HCO3- (b/c intestinal fluid has ↑HCO3-) –> hyperchloremic metabolic acidosis
  • Diarrhea –> ↓K+ (because flow rate dependent secretion of K+) –> hypokalemia
296
Q

Disorder Diarrhea

↓Surface Area for Absorption ~

A

Inflammation and Infection of Small Intestine

297
Q

Disorder Diarrhea

Osmotic Diarrhea ~

A

↑Non-absorbable solutes in lumen (example: Lactase Deficiency)

298
Q

Disorder Diarrhea

Secretory Diarrhea ~

A

↑Secretion from Crypt Cells (example: Cholera)

299
Q

Findings in Diarrhea

A
  1. ↓Mean Arterial Pressure
  2. Metabolic Acidosis
  3. Hypokalemia

GI Liver (7 decks)

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